Introduction: Migraine has been reported to be associated with an increased risk of spontaneous cervical artery dissection (sCeAD), a leading cause of ischemic stroke, particularly in young adults. Migraine may increase vulnerability to ischemia, making brain tissue more susceptible to ischemic injury. Nevertheless, migraine patients have been reported to have higher Calcitonin Gene-Related Peptide (CGRP) levels which has a vasodilatory effect that may protect against ischemia. We aim to determine if a history of migraine influences clinical presentation and outcome of sCeAD. Methods: We performed a post-hoc analysis of the STOP-CAD registry, a large international multicenter study of patients with sCeAD. Clinical, demographic, and imaging data were compared between patients with and without history of migraine applying statistical tests as appropriate for continuous variables (t-tests) and for categorical variables (Chi-square/Fisher’s exact test). Logistic regression, Kaplan-Meier survival analysis, and Cox regression with clustered standard errors were used to assess associations between migraine, sCeAD features and outcome adjusting for potential confounders. Results: STOP-CAD included 668 participants (16.6%) with a history of migraine and 3,355 (83.4%) without migraine. Patients with migraine were younger and more frequently female. In a univariate analysis, patients with migraine compared to patients without migraine had significantly fewer presentations with ischemic stroke, a higher rate of transient ischemic attacks, lower NIHSS scores at admission and better functional outcomes at discharge (mRankin<2). These results remained significant after adjusting for potential confounders: ischemic stroke (OR 0.53, 95% CI 0.42–0.67, p<0.001); NIHSS admission (OR 0.60, 95% CI 0.47–0.76, p<0.001) and mRankin<2 at discharge (OR 1.65, 95%CI 1.34-0.23, p=0.001). Conclusion: In this cohort study, migraine patients with sCeAD were significantly less likely to have an ischemic stroke at admission and had better functional outcome at discharge. Migraine might influence the clinical presentation of sCeAD and modulate the severity of cerebral ischemia. Future research should evaluate the role of potential pathophysiological mechanisms, particularly of CGRP.
Cruz et al. (Thu,) studied this question.